Electrical stimulation of nerves is widely applied in the treatment of a range of conditions and may be applied to control muscle activity or to generate sensations. Muscles and nerves may be stimulated by placing electrodes in, around, or near the muscles and nerves and by activating the electrodes by means of an implanted or external source of energy (e.g. electricity).
The diaphragm muscle provides important functions for respiration. The phrenic nerves normally transmit signals from the brain to cause the contractions of the diaphragm muscle necessary for breathing. However, various conditions can prevent appropriate signals from being delivered to the phrenic nerves. These include:                permanent or temporary injury or disease affecting the spinal cord or brain stem;        Amyotrophic Lateral Sclerosis (ALS);        decreased day or night ventilatory drive (e.g. central sleep apnea, Ondine's curse); and        decreased ventilatory drive while under the influence of anesthetic agents and/or mechanical ventilation.These conditions affect a significant number of people.        
Intubation and positive pressure mechanical ventilation (MV) may be used for periods of several hours or several days, sometimes weeks, to help critically ill patients breathe while in intensive care units (ICU). Some patients may be unable to regain voluntary breathing and thus require prolonged or permanent mechanical ventilation. Although mechanical ventilation can be initially lifesaving, it has a range of significant problems and/or side effects. Mechanical ventilation:                often causes ventilator-induced lung injury (VILI) and alveolar damage which can lead to accumulation of fluid in the lungs and increased susceptibility to infection (ventilator-associated pneumonia; VAP);        commonly requires sedation to reduce discomfort and anxiety in acutely intubated patients;        leads to rapid atrophy of the disused diaphragm muscle (ventilator-induced diaphragm dysfunction, VIDD);        can adversely affect venous return because the lungs are pressurized and the diaphragm is inactive;        interferes with eating and speaking;        requires apparatus that is not readily portable; and        increases the risk of dying if the patient fails to regain normal breathing and becomes ventilator-dependent.        
A patient who is sedated and connected to a mechanical ventilator cannot breathe normally because the central neural drive to the diaphragm and accessory respiratory muscles is suppressed. Inactivity leads to muscle disuse atrophy and an overall decline in well-being. Diaphragm muscle atrophy occurs rapidly and can be a serious problem to the patient. According to a published study in organ donor patients (Levine et al., New England Journal of Medicine, 358: 1327-1335, 2008) after only 18 to 69 hours of mechanical ventilation, all diaphragm muscle fibers had shrunk on average by 52-57%. Muscle fiber atrophy results in muscle weakness and increased fatigability. Therefore, ventilator-induced diaphragm atrophy could cause a patient to become ventilator-dependent. It has been estimated that over 600,000 US patients will be ventilator dependent and require prolonged mechanical ventilation by the year 2020 (Zilberberg et al., Critical Care Medicine, 36(5): 1451-1455, 2008).
It may also be necessary during MV to deliver or remove one or more fluids or to obtain sensor readings from within the patient. Smaller patients, such as, for example, neonates, may require smaller medical instruments to perform the aforementioned procedures. Additionally, as with any medical procedure, the risk of injury to the patient increases with the length and complexity of the medical procedure.
There remains a need for cost-effective, practical, surgically simple and minimally invasive apparatus and methods that may be applied to stimulate breathing, deliver treatment, and perform tests. There is also a need for apparatus and methods for facilitating patients on MV to regain the capacity to breathe naturally and to be weaned from MV.